健康看守的新闻与观点

多发性硬化症，蛋白质，脂肪，和孕酮

雷泥炭博士在13/02/10 1:39 PM

雷蒙德泥炭，博士

我们总是受到抗原的负担。 重要的问题，跟我们这些负担限制炎症反应的能力。

在MS多发性硬化症，它是明确的，炎症过程本身是破坏性的，雌激素是一个重要的诱发因素。 不饱和脂肪酸，膳食不平衡氨基酸相互作用与hyperestrogenism和甲状腺功能减退，产生自身免疫性退行性疾病密切。

减少炎症介质的比扩大单一抗炎剂如皮质醇。 虽然免疫抑制药物，包括“必需脂肪酸”，不减轻炎症症状暂时的，他们可能有助于病理基础。

与MS的人有长期增加皮质醇的生产。 蛋白同化失真，这将创建一个类似的营养蛋白质缺乏。 过多的血清素和雌激素引起的皮质醇生产相对不受控制。 一个恶性循环，可能会导致炎症介质和氨基酸不平衡。

抑郁症，红斑狼疮，偏头痛，更年期，糖尿病和老化有几个重要的共同点与MS的代谢功能。

流行的疗法是不合逻辑的，有可能导致病情恶化。

优质蛋白，甲状腺，孕烯醇酮和孕激素往往从根本上纠正病理。 这些都是抗炎，但他们没有免疫或代谢。

高海拔和阳光明媚的气候相关的MS的发病率较低。

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像其他自身免疫性疾病，多发性硬化症（MS），对妇女的影响往往比男性（约2比1），其在生育年龄发病（尤其是后30时，雌激素是非常高的年龄），往往加剧premenstrually ，有时缓解怀孕（Drew和查韦斯，2000年）时，孕酮是非常高的。 已发现的雌激素，孕激素的比例高的妇女，有最活跃的脑部病变（Bansil，等，1999）。 大部分的MS-肥大细胞，一氧化氮（NO），血清素，催乳素，脂质过氧化，游离脂肪酸，前列腺素和异前列，各种细胞因子参与炎症调解（白细胞介素，肿瘤坏死因子）是密切相关雌激素的行动，并在动物，自身免疫性疾病，可带来与雌激素治疗（艾哈迈德·塔拉勒）。

与雌激素的MS很强的关联，导致不合逻辑，但流行和广为宣传的医疗结论：雌激素对多发性硬化的保护，一些人声称，雌激素有利于治疗效果。 这种思维奇怪的方式其等值的想法，因为妇女是更容易比男性要开发阿尔茨海默氏症，雌激素是保护反对;或者说，因为女性有更脆弱的骨头比男人，和他们的进步骨损失发生在他们的最大暴露于雌激素的时代，雌激素预防骨质疏松。

在这个医疗环境，是公认的雌激素和退化性疾病之间的密切关联，但他们说，协会的出现是因为没有足够的雌激素的意义有悖常理。 炉灶燃烧，因为它是不够热。

正如戴维·巴里说，我不是做这个。 最近广为人知的文章已经表明，雌激素可以保护大脑（甚至预防中风！），因为它增加血清素和NO [一氧化氮]。 也有一些是几乎美观顺眼这么多的重大错误时，集中到一个单一的文章。 一氧化氮和羟色胺的神经毒性（Joseph，等，1991; Skaper，等，1996;帕金森等，1997;，圣地亚哥等人，1998年。巴杰尔，等，2000），抑制线粒体呼吸的结果。 NO发挥了重要作用脂质过氧化和脱髓鞘。 有趣的是看到羟色胺和没有公开相关的雌激素，其已仔细从公众视线中隐藏的线粒体毒性。

关于MS的旧理论，有关的基因和病毒，细菌，维生素缺乏，石油不足，毒药，要接种疫苗的反应（尤其是B型肝炎及流感）的新理论的原因有以下几种学说。 已放弃唯一的理论是19世纪的有关精神论“歇斯底里瘫痪，”虽然偶尔有人还在谈论情绪多发性硬化症的原因，“女性歇斯底里”一词已演变为“转化症。”

每一个主要的理论有几个事实似乎支持，但忽略了许多其他事实。 大家都同意，在MS以某种方式参与免疫系统，但是这确实问题出在哪里开始，因为这个想法，炎症是一种内在的免疫力。 炎症如果“是必要的和好”，那么它​​成为一个问题准确定义之间的边界是一个适当的反应和退化过程。 在良好的光线，可以看到水肿，降低细胞呼吸，丧失正常功能，其不同程度的纤维化，炎症的每个组件的一部分作为“防御性免疫反应。”当组织损伤导致修复，“必须”被看作是有益的，即使它会导致在功能组织的地方形成疤痕，因为比较是一个想象的最坏的结果，一个不完美的恢复，而不是比较的可能性，潜在的有害炎症过程剂可能有做没有坏处。

炎症如何与生物体的资源最简单的例证是血糖变化，而变化从轻度刺激性潜在致命的化学物质，动物暴露实验。 当动物有非常低血糖，温和的刺激可能是致命的，但是当其血糖保持非常高的，甚至是致命的抗原只有轻度刺激性。 不同的血液中钠离子浓度相似，但较弱，影响。

有一种倾向，不仅看到了作为一个正常的免疫炎症，但要看到它作为抗原的性质成正比，除时，免疫系统已被引为它以前接触，在这种情况下，机体所有（要么没有反应，因为它已成为免疫），或反应会更猛烈，比它的第一次接触，因为它已成为过敏。 但是，在现实中，只是血液中的葡萄糖和钠浓度（甲状腺，和许多其他物质不被认为是免疫系统的一部分），可以在“免疫”反应程度的巨大差异。

在过于敏感的条件下产生的低血糖，几件事情发生有助于不适应夸张的炎症反应的。

肾上腺素增加，低血糖，如果肾上腺素失败糖原转化为葡萄糖，它会提供从脂肪细胞中解放出来的自由脂肪酸替代燃料。

如果解放的不饱和脂肪酸，它们会导致血清素分泌，血清素和不饱和脂肪酸会抑制线粒体呼吸，加剧了低血糖。 它们会刺激细胞因子的释放，激活多种免疫和炎症过程，他们会导致血管渗漏，创造水肿和纤维化的第一阶段开始。 肾上腺素和血清素会刺激释放皮质醇，从大骨骼肌等组织动员的氨基酸。 这些肌肉中含有大量的半胱氨酸和色氨酸，其中，除其他作用，抑制甲状腺。 色氨酸的增加，尤其是在游离脂肪酸的存在，是有可能被转换成额外的羟色胺，脂肪酸释放白蛋白色氨酸进入大脑，提高其入境。 游离脂肪酸和增加血清素，减少代谢效率（例如，导致胰岛素抵抗）和促进炎症状态。

脂肪在血液流很容易进入到大脑，和不饱和游离脂肪酸产生脑水肿（陈等人，1983年，1988年）。 当血管渗漏引起的脑水肿，通常被排除的蛋白质可以进入。 刺激，兴奋和疲惫的大脑交流谷氨酰胺色氨酸，加速其从血液中摄取。

当组织受伤或强调，应对该组织的改变组件形成抗体。 因此，我们可以调用挫伤或扭伤是一种自身免疫性条件，但有没有商业撞伤，胫抗体测试。 的特异性抗体测试的情况下，似乎是在归类为自身免疫性条件，如要素“自身免疫性甲状腺炎。”不幸的是，这种方式使用的语言是嵌套在一个文化，是因果关系的不切实际的想法，还有数千人上搜索“突变基因是负责疾病”，并为纠正缺陷的药物，将建立自己的职业生涯。

早在免疫学的研究，重点是抗体。 甚至更早，炎症已经概念化的“幽默”，和其他前科学思想。 尽快多发性硬化症/歇斯底里麻痹被列为一种自身免疫性疾病，免疫系统的性质有关的原始想法相互作用有关的性质和大脑细胞的结构与原始的想法，什么病的各种理论混合是。

而非看到免疫神经损伤多发性硬化症的所有其他功能的原因，我认为，重要的是看上下文中解释神经的事件，在一些条件的一般特征。

它一直被称为MS的发病率增加与赤道的距离往往很长一段时间。 在阳光明媚的气候干燥，并在高海拔地区低发病率。 两个清晰的膳食影响已发现：吃猪肉，马肉。

与MS的人不很好调节自己的体温。 他们的神经传导速度很慢，在正常的人，传导是在较高温度下更快，但在人与MS传导速度比正常温度在98.6度的F在较低温度下。 低于正常温度也与老年，更年期的潮热。

脑葡萄糖代谢的多发性硬化症是非常低的，在我自己的观察，一般代谢率低于正常。 然而，有些人的原因造成的代谢低下的病灶，而不是反之亦然。

缺乏的不饱和脂肪酸的动物，有较高的代谢率和利用葡萄糖的能力，将其转换为二氧化碳更容易，有一个更大的抗毒素（哈里斯等人，1990年甚至是眼镜蛇毒液。Morganroth，等， 1989年），包括内毒素（李等人，1990年），防止过度的血管渗漏和免疫损伤（高桥等人，1992年），和创伤，他们的肌肉反应速度加快而快速抽搐肌肉少容易疲倦（艾雅和Hulber，1996）。

在与MS的人，血液更粘稠，血小板易于聚集在一起更容易。 他们的皮质醇水平高于正常，和他们 - 垂体 - 肾上腺皮质激素是难以抑制。 这是一个条件，也看到在抑郁症和老年。 尽管皮质醇的长期升高，与MS的人通常有低血糖。 他们偶尔发现有低钠血症，低血钠，但这是难以确定时，血液中的水分含量是可变的。 他们的催乳激素可能会很高，这可能会导致高雌激素，血清素高，低钠盐，或低甲状腺。 喝太多水可以增加催乳素，并能损害神经的髓鞘外壳过多的血清素，往往造成过量饮酒。 血糖，钠和水含量的干扰可以破坏大脑的髓鞘结构。 高雌激素会干扰血液渗透，使得它保留溶质的水太多，并与许多雌激素的影响的关系，因为简单的渗透压变化可以破坏的髓鞘结构，它似乎，这个机制应该被调查的深入之前，它是假定免疫活动是主要的。

肥大细胞，促进炎症释放物质如组胺和5 - 羟色胺（使血管渗漏），比正常的大脑更在许多多发性硬化症脑。 由于血小板凝结释放血清素，而且还因为建议 - 羟色胺过剩是由许多其他功能的MS，血清素拮抗剂（昂丹司琼和酮色林，例如）已成功地用于治疗。

雌激素会导致肥大细胞释放炎症介质，它会导致血小板聚集，释放他们的血清素。 由于雌激素的优势是存在活跃的脑部病变密切相关，抗雌激素治疗，似乎是显而易见的，在MS。 孕激素对抗雌激素对肥大细胞和血小板的影响。

阿司匹林防止各种炎症过程，但它是最著名的抑制前列腺素的。 而阿司匹林常被用来减轻疼痛在MS，另一种前列腺素合成酶抑制剂，消炎痛，已被用于在MS治疗，它似乎是适当的，更仔细地探讨阿司匹林在防止或减轻MS的可能发挥的作用。

一个简单的蛋白质缺乏症有许多令人惊讶的效果。 它降低体温，并抑制甲状腺，但它增加了炎症和血液凝块的趋势。 由于大脑和心脏和肺需要连续供应的必需氨基酸，如果他们继续运作，膳食蛋白质的情况下，产生皮质醇，必须不断的消耗性组织，主要是骨骼肌氨基酸动员。 这些肌肉有高浓度的色氨酸和半胱氨酸，从而抑制甲状腺。 半胱氨酸是excitoxic的，和色氨酸是羟色胺的前体。 据推测，他们的存在，诱导应力释放，肌肉是在某些类型的压力，减少代谢活性的机制之一。

当怀孕的动物蛋白质被剥夺，新生动物有异常高的水平，血清素，负责，过量的酶倾向于保持多余的，即使他们都已经长大，有足够的蛋白质 - 羟色胺。 这是类似于过剩的雌激素的影响早在生活中，创建一个趋势，以发展在成年后乳腺癌或前列腺癌。 妊娠期的经验，例如，怀孕和出生体重长的人谁后开发的MS，这将是有趣的研究。

虽然在北部国家的人是不正常蛋白质匮乏，他们往往得到了他们的蛋白质的肌肉的很大一部分。 在传统文化中，所有食品动物部分食用鸡的脚，头，脖子，动物的耳朵和眼球等，使氨基酸平衡良好，保持了较高的代谢率，防止压力。

多发性硬化症是猪肉和马肉的消费，而不是牛肉，羊肉，或山羊，观察是非常有趣的，因为这些动物的脂肪基本上是一样的，他们吃的植物材料的脂肪，这意味着它亚油酸和亚麻酸是非常高的。 牛，绵羊和山羊瘤胃中包含细菌，转换​​成更多的饱和脂肪多不饱和脂肪。 不饱和脂肪抑制酶消化蛋白质，MS患者已报告有肉的消化不好古普塔等人（1977）。

多不饱和脂肪本身是线粒体毒性，抑制葡萄糖氧化，抑制甲状腺功能，氧化葡萄糖的能力上具有相同的抑制作用，但他们也已经打开，enzymically，到前列腺和非-enzymically的，自发性脂质过氧化，变成有毒的异前列。 异前列，一些前列腺素，升高与MS的人的大脑和其他组织。

多发性硬化症是非常高的脂质过氧化。 一氧化氮（其合成的雌激素在大脑的大部分地区推广）是激活过氧化自由基。

脂质过氧化选择性破坏，自然不稳定的多不饱和脂肪。 在动脉粥样硬化，血管斑块中含有不饱和脂肪很少。 这是因为它们过氧化如此迅速，但其饱和不饱和脂肪的比例高，已被用来论证，多不饱和油“保护心脏。”类似的论点往往在MS，虽然一些研究不支持这一想法是有任何的不饱和脂肪的缺乏。 由于脂质过氧化是非常高的，这将是合理的假设，有丰富的多不饱和脂肪过氧化反应，通过催化剂，如铁（SM莱文，1997年）和一氧化氮和peroxynitrile。

我相信，所以往往在与MS的人热不容忍现象的一个重要方面可能相对热疗释放到血液中的游离脂肪酸增加的趋势。 妇女，由于雌激素的影响，通常比男人血液中的游离脂肪酸的水平要高得多。 雌激素增加释放游离脂肪酸从脂肪储存，不饱和脂肪与雌激素和催乳素增效，提高他们的影响。

温度调节显然涉及一些感温度非常准确的神经细胞，并相应地改变他们的活动。 水有非常高的热容量，这意味着它需要相对大量的热量，以改变其温度。 “消失的热量被消耗在水的结构性变化。 蛋白质有同类型结构复杂，水和他们一起可以做出有效的温度传感器，“温度计”。（其他物质往往发生重大的结构性变化，只因为他们熔化或汽化。著名的“液态晶体”，有几个不同的结构阶段，但细胞质就像是一个非常微妙的液晶）。“调温细胞”实际上是回应到一定程度的内部结构，而不是抽象的温度。 这样的事情，改变其内部结构，将修改其温度设定点。“

增加雌激素会导致动物，以降低其温度，它可能增加“结构温度”恒温细胞，“融化”，其内部结构。 孕激素引起的动物，以提高其温度，它显然没有结构，增加/减少温度的恒温细胞结构。 如果你把冰温控器，房间变热。

一个细胞的内部结构，相当于其准备工作。 疲劳稍微“融化”的细胞的状态，在这种结构似乎已消耗化学能源储备。 实验表明这种影响是非常明确的，但他们被忽略，因为它们不符合人的细胞的刻板想法。 有了一个非常敏感的温度计，它可以测量由神经所产生的热量，当它受到刺激。 这并不奇怪。 但它是令人惊讶，神经刺激复苏时，它从它的环境中吸收热量，降低局部温度。 ，甚至侵犯了一些人的概念“熵”，但它可以很容易地被证明，改变某些材料的形式改变了它们的热容量，当橡皮筋被拉长，它也变热，或合同，它变得凉爽。

的excitants，雌激素和皮质醇，减缓神经的传导，因为它们会导致其内部结构将消散。 他们创造了“预疲劳”状态中的细胞。

森特 - Gyorgyi兔心实验，表明，雌激素减少心脏的准备工作，孕激素增加的准备工作，和他说，它没有通过这种“建筑结构。”他指出，为1给予药物或其他的刺激，细胞有一个特点，响应，成为或者更多的激活或抑制，但他表明，正常的浓度或强度范围的刺激外，细胞的反应往往是扭转。

如果是这样的情况在MS的神经，它解释了奇怪的行为，在升温的神经，降低其功能。 言下之意是，内部结构（能源）必须恢复到的神经。 在我所描述的，在以前的通讯，钠，ATP，二氧化碳和孕激素增加，增加镁钙比，实验中已经发现，增加细胞的能量和结构。 甲状腺激素是最终负责维持细胞的能量和结构，并响应，但是，如果它不允许所有其他因素调整的情况下突然增加，这将提高温度，太突然。 它不需要花费很长时间，但所有的因素都必须在同一时间出席。

血清素，褪黑激素，雌激素，多不饱和脂肪都倾向于降低体温。 由于雌激素和不饱和脂肪蜂窝excitants，在实际体温下降有助于抵消他们的兴奋作用。

无论是明亮的光线和高海拔倾向于降低血清素的影响。 该组织保留在高海拔地区的二氧化碳减少了许多疾病的发病率，心脏疾病和癌症，多发性硬化症，可能会受到影响。 据了解，二氧化碳在参与髓鞘的调节自身的含水量。 换气过度，造成损失的二氧化碳，释放组胺和血清素，使血液更粘稠，同时使血管渗透，并导致他们收缩。

如果用MS的人过多的雌激素，血清素，不饱和脂肪，铁，水，和缺乏甲状腺，缺乏孕烯醇酮生产中的髓鞘形成细胞（少突胶质细胞）的相互作用，通过开发，有很多事情可以做停止其进展情况，并有可能扭转这种局面。

由于温度突然升高会释放促炎症脂肪的数量增加，事情应该逐步改变。 增加盐是热的，但镁是增加对热疗的保护，所以增加镁（泻盐浴池，例如，咖啡，水果，一些蔬菜和肉类）会很有帮助。 镁正在迅速失去细胞中的甲状腺功能减退。 糖，脂肪和矿物质的陪同，在牛奶中，需要以较低的皮质醇，并维持甲状腺的活动。 均衡的蛋白质，如奶酪，土豆，鸡蛋，牛肉或羊肉，肉汤（明胶和矿物质含量特别），防止色氨酸过剩，抑制甲状腺，可能是一种神经毒素。 饱和脂肪，经常使用，减少直接的毒性中的不饱和脂肪的抗代谢作用，但它需要较长的时间来改变脂肪储存余额。

由于阿司匹林降低温度，抗炎，抗雌激素在某些情况下，是一种强大的抗氧化剂，它很可能，这将缓解症状和防止MS的进展，因为它在其他退行性疾病。 由于血小板聚集可能是参与炎症的重点，阿司匹林可能有助于防止形成新领域损害。

虽然是其抗炎作用的糖皮质激素，皮质醇被称为促进杀死脑细胞的兴奋。 由于雌激素减少GABA的，雌激素和血清素激活兴奋性氨基酸递质，除了预先存在皮质醇过多的合成糖皮质激素是除了发炎地区可能损害大脑的部分。

多余的皮质醇，抑郁症的老人，和hyperestrogenism往往归结与甲状腺补充剂的使用，但孕烯醇酮有非常直接的行动（在反对 - 羟色胺），可以安静的垂体，减少促肾上腺皮质激素和皮质醇。 黄体酮有一些类似的效果，是对多余的皮质醇保护，是一种在神经和大脑恢复的主要因素。 甲状腺，孕激素和孕烯醇酮都参与新髓鞘的形成，并在预防水肿，损害。

由于甲状腺和孕激素，减少雌激素的发炎组织的形成，而皮质醇刺激其形成的，它似乎明智地使用其直接的抗炎作用，其中包括抑制NO的生成（Drew和查韦斯，2000年）的甲状腺和孕激素，他们缺乏的兴奋，雌激素刺激的糖皮质激素的影响。 而糖皮质激素是从肌肉分解，并释放出的半胱氨酸和色氨酸，甲状腺和孕激素代谢，并防止这些氨基酸的毒性后果。

参考

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J Mol Med 1997 Mar;75(3):174-86. The role of nitric oxide in multiple sclerosis. Parkinson JF, Mitrovic B, Merrill JE “Elevated nitric oxide bio-synthesis has been associated with nonspecific immune-mediated cellular cytotoxicity and the pathogenesis of chronic, inflammatory autoimmune diseases including rheumatoid arthritis, insulin-dependent diabetes, inflammatory bowel disease, and multiple sclerosis.”

Fed Proc 1987 Jan;46(1):91-6. Role of the clotting system in the pathogenesis of neuroimmunologic disease. Paterson PY, Koh CS, Kwaan HC “Our studies of the clotting system and ensuing fibrinolysis implicate coagulation and cleavage of fibrin within or on the luminal surface of the cerebrovasculature as events initiating the inflammation characterizing EAE.” “We postulate that the critical event precipitating EAE is binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuing fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides cleaved from fibrin open the BBB, thereby setting the stage for the cascade of inflammatory events culminating in clinical manifestations of EAE.”

Neurotoxicology 1998 Aug-Oct;19 (4-5):599-603. In vitro effect of the cysteine metabolites homocysteic acid, homocysteine and cysteic acid upon human neuronal cell lines. Parsons RB, Waring RH, Ramsden DB, Williams AC “Cysteine (CYS) is a non-essential amino acid which elicits excitotoxic properties via the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor.. CYS levels are known to be elevated in association with neurological disease such as Alzheimers Disease (AD) and Parkinsons Disease (PD).” “These results show that toxic responses are cell-type specific for CYS and its metabolites and this may be reflected in the patterns of neurodegeneration observed in such diseases as AD and PD.”

WMJ 1983 Mar-Apr;55(2):146-50. [Effect of tryptophan excess in a diet on amino acid composition of skin collagen and on an initial stage of protein biosynthesis in rat liver]. Pechenova TN, Sushkova VV, Solodova EV, Gulyi MF Protein deficiency and tryptophane load against its background lead to the acid-soluble collagen synthesis in the rat skin. The amino acid composition of the collagen differs from the norm. This is accompanied by changes in the free amino acid pool of blood serum and liver, under tryptophane load the free amino acids pool of the liver increasing twice as high. At the same time protein deficiency increases and tryptophane load decreases the level of tRNA amino acylation with tryptophane in the animal liver. Thus, protein deficiency and tryptophane load against its background cause deep changes in the protein biosynthesis.

Fed Proc 1987 Jan;46(1):91-6. Role of the clotting system in the pathogenesis of neuroimmunologic disease. Paterson PY, Koh CS, Kwaan HC “Our studies of the clotting system and ensuing fibrinolysis implicate coagulation and cleavage of fibrin within or on the luminal surface of the cerebrovasculature as events initiating the inflammation characterizing EAE.” “We postulate that the critical event precipitating EAE is binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuing fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides cleaved from fibrin open the BBB, thereby setting the stage for the cascade of inflammatory events culminating in clinical manifestations of EAE.”

Rev Esp Fisiol 1983 Mar;39(1):39-44. Intralipid and free plasmatic tryptophan in vitro. Pena JM, Aulesa C, Vinas O, Bosch J, Farriol M, Schwartz S “In an attempt to investigate the role of the lipidic emulsion Intralipid in the development of metabolic encephalopathy in a patient showing high free tryptophan levels, the relationship between lipidic emulsion and free tryptophan was examined in in vitro experiments. The addition of intralipid to normal serum produces an immediate increase in non-esterified fatty acids and a parallel rise in free tryptophan. Moreover, when serum with intralipid is incubated at 37 degrees C, the lipases release new non-esterified fatty acids and the free tryptophan increases proportionally.” “It is concluded that intralipid causes an increase in free tryptophan levels. It is known that in vivo free tryptophan modulates 5-hydroxytryptamine synthesis and thus may be considered a possible causal agent for encephalopathy.”

Med Hypotheses 1980 May;6(5):545-557. Fatty acids, fibrinogen and blood flow: a general mechanism for hyperfibrinogenemia and its pathologic consequences. Pickart LR, Thaler MM Plasma fibrinogen is elevated in various stressful states and conditions in which active mobilization of free fatty acids (FFA) occurs. Reduction of plasma FFA by an assortment of hypolipidemic drugs is consistently followed by a decrease in the accompanying hyperfibrinogenemia. A direct link between FFA and fibrinogen has been demonstrated in animals, and in experiments employing incubated liver slices. Based on these clinical and experimental observations, we postulate that hepatic fibrinogen synthesis is stimulated by FFA. Since fibrinogen is a major determinant of whole blood viscosity, erythrocyte aggregation, and sludging of red cells in terminal and pre-terminal blood vessels, we propose that microcirculatory blood flow may be impaired in the presence of chronically elevated plasma FFA levls. Consequently, hypolipidemic drugs may be effective in prevention of circulatory complications associated with FFA-induced hyperfibrinogenemia.

Neurologia 1996 Aug-Sep;11(7):272. [Exacerbation of spasticity induced by serotonin reuptake inhibitors. Letter]. del Real MA, Hernandez A, Vaamonde J, Gudin M

J Neurol Neurosurg Psychiatry 1997 Mar;62(3):282-4. Ondansetron, a 5-HT3 antagonist, improves cerebellar tremor. Rice GP, Lesaux J, Vandervoort P, Macewan L, Ebers GC. “It has been previously shown that ondansetron, a 5-HT3 antagonist, can ameliorate vertigo in patients with acute brainstem disorders. A coincidental benefit was the improvement of cerebellar tremor in some patients with both vertigo and tremor. To further evaluate this effect, a placebo controlled, double blind, crossover study was conducted of a single dose of intravenous ondansetron in 20 patients with cerebellar tremor caused by multiple sclerosis, cerebellar degeneration, or drug toxicity.” “Thirteen of 19 patients were deemed to have improved spiral copying after treatment with ondansetron when compared with baseline performance.”

Neurologia 1993 Oct;8(8):252-5. [Retinal periphlebitis in multiple sclerosis. A prospective study]. Rio J, Colin A, Salvador F, Tintore M, Viguera ML, Montalban J, Codina A “In three cases (12.5%) retinal periphlebitis was observed.” “Given the absence of myelin in the retina, the presence of retinal periphlebitis suggests the existence of a vascular mechanism in the pathogenesis of multiple sclerosis.”

Int J Neurosci 1995 Dec;83(3-4):187-98. Premenstrual exacerbation of symptoms in multiple sclerosis is attenuated by treatment with weak electromagnetic fields. Sandyk R. “The present report concerns two women with chronic progressive stage MS who experienced, coincident with increasing functional disability, regular worsening of their symptoms beginning about a week before menstruation and abating with the onset of menstruation. These symptoms resolved two months after the initiation of treatment with EMFs.”

J Physiol Biochem 1998 Dec;54(4):229-37. The role of nitric oxide in the pathogenesis of multiple sclerosis. Santiago E, Perez-Mediavilla LA, Lopez-Moratalla N “The inducible NOS (iNOS) is associated with the development of a number of autoimmune diseases.” “Induction of the enzyme is effected by proinflammatory cytokines, immunomodulating peptides, and even beta-endorphin through a mechanism involving an increase in cAMP. An excessive production of NO has been implicated in the severe lesions observed in multiple sclerosis (MS).”

J Neurol 1980 Jan;222(3):177-82. Cerebrospinal fluid lipids in demyelinating disease. 二。 Linoleic acid as an index of impaired blood-CSF barrier. Seidel D, Heipertz R, Weisner B “The linoleic acid content of control CSF (1.6 +/- 0.8 nMol/ml) is considerably lower than the corresponding serum value (2.5–4.1 muMol/ml). Although CSF from MS patients contains a significantly higher linoleic acid concentration than controls the close correlation between CSF linoleic acid and CSF albumin is maintained. The high CSF concentration of cholesterol esters rich in linoleic acid, which are abundant in serum but represent only traces in CNS lipids, points towards an impaired BBB function as the cause of CSF linoleic increase. We are able to show that both albumin and linoleic acid are suitable as “serum markers….”

J Neurol Sci 1987 Feb;77(2-3):147-52. Chronic periphlebitis retinae in multiple sclerosis. A histopathological study. Shaw PJ, Smith NM, Ince PG, Bates D Retinal periphlebitis in multiple sclerosis is of particular interest in relation to our understanding of the pathogenesis of the demyelinating central nervous system plaques. Previous studies have largely been clinical, and there is little detailed histopathological information relating to this condition. We present the first detailed report in the neurological literature on the histological findings in chronic periphlebitis retinae associated with multiple sclerosis. The most significant abnormalities of the affected retinal veins were the presence of thick laminated collagen in the wall, associated with a scanty infiltration of plasma cells.

Am Heart J 2000 Aug;140(2):212-8. Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease. Shechter M, Merz CN, Rude RK, Paul Labrador MJ, Meisel SR, Shah PK, Kaul S.

J Neurochem 1996 Mar;66(3):1157-66. Mast cell activation causes delayed neurodegeneration in mixed hippocampal cultures via the nitric oxide pathway. Skaper SD, Facci L, Romanello S, Leon A. “Neurotoxicity required a prolonged period (12 h) of mast cell incubation, and appeared to depend largely on elaboration of the free radical nitric oxide by astrocytes.” “Myelin basic protein and 17 beta-estradiol had a synergistic action on the induction of mast cell-associated neuronal injury.” “Further, palmitoylethanolamide, which has been reported to reduce mast cell activation by a local autacoid mechanism, decreased neuron loss resulting from mast cell stimulation in the mixed cultures but not that caused by direct cytokine induction of astrocytic nitric oxide synthase.” “These results support the notion that brain mast cells could participate in the pathophysiology of chronic neurodegenerative and inflammatory diseases of the nervous system, and suggest that down-modulation of mast cell activation in such conditions could be of therapeutic benefit.”

International Journal of Microcirculation–Clinical and Experimental, 1996, Vol 16, Iss 5, pp 266-270. Hyperventilation enhances transcapillary diffusion of sodium fluorescein. J Steurer, D Schiesser, C Stey, W Vetter, MV Elzi, JP Barras, UK Franzeck. “Voluntary hyperventilation (HV) provokes hemoconcentration due to a loss of fluid from the intravascular space.” “The exact, mechanism of enhanced transcapillary diffusion of Na fluorescein is not known, The distinct increase in FLI without a significant change in microvascular skin flux suggests an HV-induced increase in capillary pressure or an enhancement in capillary permeability for water and small solutes.”

Kidney Int 1992 May;41(5):1245-53. Essential fatty acid deficiency normalizes function and histology in rat nephrotoxic nephritis. Takahashi K, Kato T, Schreiner GF, Ebert J, Badr KF.

Arthritis Rheum 1981 Aug;24 (8):1054-6. Sex steroid hormones and systemic lupus erythematosus. Talal N.

Clin Rheum Dis 1982 Apr;8(1):23-8. Sex hormones and modulation of immune response in SLE. Talal N.

Ann NY Acad Sci 1986;475:320-8. Hormonal approaches to immunotherapy of autoimmune disease. Talal N, Ahmed SA, Dauphinee M.

Ann Nucl Med 1998 Apr;12(2):89-94. Clinical significance of reduced cerebral metabolism in multiple sclerosis: a combined PET and MRI study. Sun X, Tanaka M, Kondo S, Okamoto K, Hirai S “The severity of cerebral hypometabolism was also related to the number of relapses.” “Our results suggest that measurement of cerebral metabolism in MS has the potential to be an objective marker for monitoring disease activity and to provide prognostic information.”

Fed Proc 1987 Jan;46(1):118-26. Pathway to carrageenan-induced inflammation in the hind limb of the rat. Vinegar R, Truax JF, Selph JL, Johnston PR, Venable AL, McKenzie KK “Antiserotonin agents inhibited the hypoalgesia and part of the edema. These findings and histological observations suggested that dermal mast cells were injured by C. The hyperalgesia and part of the edema were sensitive to arachidonate cyclooxygenase inhibitors (AACOIs). It is speculated that injured mast cells metabolize arachidonic acid and reactive intermediates, not prostaglandins, mediate the NPIR hyperalgesia and part of the edema.” “Arachidonic acid metabolism by neutrophils is speculated to produce the mediators of phagocytic inflammatory (PI) edema and hyperalgesia.”